DNA Methylation Profiling Reveals the Change of Inflammation-Associated ZC3H12D in Leukoaraiosis

Huang, Wenyan; Yi, Ke-Hui; Li, Zhi; Wang, Han; Li, Mingli; Cai, Lun; Lin, Hongyang; Lin, Qing; Tzeng, Chi-Meng

doi:10.3389/fnagi.2018.00143

Cited by 14 publications

(16 citation statements)

References 61 publications

(87 reference statements)

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“…In the early stages of the development of the central nervous system, DNA methylation may play an essential role. It is reported that DNA methylation regulates the differentiation of neurons, which is closely related to adult learning, memory, and cognition [32]. During the process of DNA methylation changes, it is easy to cause more epigenetic diseases due to other factors such as the environment.…”

Section: Discussionmentioning

confidence: 99%

Abnormal DNA Methylation in Thoracic Spinal Cord Tissue Following Transection Injury

et al. 2018

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Background Spinal cord injury (SCI) is a serious disease with high disability and mortality rates, with no effective therapeutic strategies available. In SCI, abnormal DNA methylation is considered to be associated with axonal regeneration and cell proliferation. However, the roles of key genes in potential molecular mechanisms of SCI are not clear. Material/Methods Subacute spinal cord injury models were established in Wistar rats. Histological observations and motor function assessments were performed separately. Whole-genome bisulfite sequencing (WGBS) was used to detect the methylation of genes. Gene ontology (GO) term enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were performed using the DAVID database. Protein–protein interaction (PPI) networks were analyzed by Cytoscape software. Results After SCI, many cavities, areas of necrotic tissue, and many inflammatory cells were observed, and motor function scores were low. After the whole-genome bisulfite sequencing, approximately 96 DMGs were screened, of which 50 were hypermethylated genes and 46 were hypomethylated genes. KEGG pathway analysis highlighted the Axon Guidance pathway, Endocytosis pathway, T cell receptor signaling pathway, and Hippo signaling pathway. Expression patterns of hypermethylated genes and hypomethylated genes detected by qRT-PCR were the opposite of WGBS data, and the difference was significant. Conclusions Abnormal methylated genes and key signaling pathways involved in spinal cord injury were identified through histological observation, behavioral assessment, and bioinformatics analysis. This research can serve as a source of additional information to expand understanding of spinal cord-induced epigenetic changes.

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Section: Discussionmentioning

confidence: 99%

Abnormal DNA Methylation in Thoracic Spinal Cord Tissue Following Transection Injury

et al. 2018

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“…Chronic inflammation has been shown to be closely associated with aging-associated pathologies, and interestingly, each of these is strongly correlated with epigenetic alteration [ 43 , 44 ]. There is growing evidence that epigenetic mechanisms may underlie the development of aging-associated chronic diseases and may mediate the effects of nutrition.…”

Section: Introductionmentioning

confidence: 99%

Polyamine Metabolism and Gene Methylation in Conjunction with One-Carbon Metabolism

Soda

2018

IJMS

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Recent investigations have revealed that changes in DNA methylation status play an important role in aging-associated pathologies and lifespan. The methylation of DNA is regulated by DNA methyltransferases (DNMT1, DNMT3a, and DNMT3b) in the presence of S-adenosylmethionine (SAM), which serves as a methyl group donor. Increased availability of SAM enhances DNMT activity, while its metabolites, S-adenosyl-l-homocysteine (SAH) and decarboxylated S-adenosylmethionine (dcSAM), act to inhibit DNMT activity. SAH, which is converted from SAM by adding a methyl group to cytosine residues in DNA, is an intermediate precursor of homocysteine. dcSAM, converted from SAM by the enzymatic activity of adenosylmethionine decarboxylase, provides an aminopropyl group to synthesize the polyamines spermine and spermidine. Increased homocysteine levels are a significant risk factor for the development of a wide range of conditions, including cardiovascular diseases. However, successful homocysteine-lowering treatment by vitamins (B6, B12, and folate) failed to improve these conditions. Long-term increased polyamine intake elevated blood spermine levels and inhibited aging-associated pathologies in mice and humans. Spermine reversed changes (increased dcSAM, decreased DNMT activity, aberrant DNA methylation, and proinflammatory status) induced by the inhibition of ornithine decarboxylase. The relation between polyamine metabolism, one-carbon metabolism, DNA methylation, and the biological mechanism of spermine-induced lifespan extension is discussed.

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“…ZC3H12C could inhibit vascular in ammation and proin ammatory gene expression in endothelial cells [46] and regulate proin ammatory activation of macrophages [47,48]. ZC3H12D contributed to in ammation-associated signaling pathways involved in the pathogenesis of Leukoaraiosis [49]. BOP1 could prompt cell migration and invasion in colorectal cancer [50] and loss of BOP1 conferred resistance to BRAF kinase inhibitors in melanoma [51].…”

Section: Discussionmentioning

confidence: 99%

Identification and Validation of an RNA Binding Proteins-Associated Prognostic Signature for Non-Small Cell Lung Cancer

Miao¹,

Chen

Xiao

et al. 2020

Preprint

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Background: Non-small cell lung cancer (NSCLC) is a malignancy with relatively high incidence and poor prognosis. RNA-binding proteins (RBPs) were reported to be dysregulated in multiple cancers and were closely associated with tumor initiation and progression. However, the functions of RBPs in NSCLC remain unclear. Method: The RNA sequencing data and corresponding clinical information of NSCLC was downloaded from The Cancer Genome Atlas (TCGA) database. We identified aberrantly expressed RBPs between tumor and control tissue, and systemically investigated the expression and prognostic value of these RBPs by a series of bioinformatics analysis.Results: A total of 459 aberrantly expressed RBPs (291 up-regulated and 168 down-regulated RBPs) were identified. Functional enrichment analysis indicated that the differentially expressed RBPs were mainly associated with RNA splicing, ncRNA metabolic process, regulation of translation, mRNA surveillance pathway, RNA degradation, and RNA transport. Thirteen RBPs (ZC3H12C, ZC3H12D, BOP1, CASC3, DDX24, IGF2BP1, KHDC1, FASTKD3, TARBP1, INTS7, NOL12, SNRPB, PABPC1L) were identified as prognostic RBPs by multivariate Cox regression analysis, and were used to construct a prognostic signature. Further analysis demonstrated that high-risk group were significantly related to poor overall survival in training and testing cohort. The area under receiver operator characteristic curve of the prognostic signature was 0.703 in training cohort and 0.636 in testing cohort. In addition, the prognostic signature was further validated in differently clinical subgroup (>=65, <65, female, male, stage I-II, III- IV, T1-2, T3-4, N0, N1-3, M0 and M1). The risk score was an independent prognostic factor of NSCLC. A nomogram based on thirteen RBPs was constructed to predict the survival of patients.Conclusion: Our results provide novel insights into the pathogenesis of NSCLC. The RBPs-associated prognostic signature showed predictive value for NSCLC prognosis, with potential applications in clinical decision-making and individualized treatment.

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DNA Methylation Profiling Reveals the Change of Inflammation-Associated ZC3H12D in Leukoaraiosis

Cited by 14 publications

References 61 publications

Abnormal DNA Methylation in Thoracic Spinal Cord Tissue Following Transection Injury

Abnormal DNA Methylation in Thoracic Spinal Cord Tissue Following Transection Injury

Polyamine Metabolism and Gene Methylation in Conjunction with One-Carbon Metabolism

Identification and Validation of an RNA Binding Proteins-Associated Prognostic Signature for Non-Small Cell Lung Cancer

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